Genomic evolution of sickle cell individual to Malaria
Introduction Plasmodium falciparum is a mosquito parasite that causes malaria mostly in tropical and subtropical regions. it is estimated that approximately 1 million people are killed each year as a result of malaria. Natural selection, allow the evolutionary propagation of alleles that confer survival advantage to certain individuals in populations against malaria parasite. Individuals in a population with detrimental phenotypes are subject to extinction. For instance, sickle cell anemia individuals with a recessive homozygote alleles and individuals with a normal homozygous alleles are more susceptible to Plasmodium falciparum ''a malaria parasite and subject to death from malaria. While heterozygote sickle cell carrier have an inherited advantage that confer certain level of resistance to malaria parasite,survival and higher reproduction rate due to the short life span of their red blood cell and inhibiting P.falciparum life cycle. Sickle Cell anemia a common form of sickle cell disease, is an autosomal recessive disorder that is characterized by sickle shaped red blood cell with a short life span, anemia, fatigue, joint pain, a swollen spleen, severe infections, stunted growth and immunosuppression. Cause of malaria ''Plasmodium falciparum is the causative agent of life-threatening malaria, transmitted by female anopheles mosquito.'' P. Falciparum is prevalent in prevalent in tropical and subtropical regions. The stages of stages in the life cycle of ''Plasmodium, including sporozoites , merozoites, and gametocytes. When an infected female anopheles mosquito feeds on human blood and in the process transmit or inject the P.faciparum into the host red blood cell via bite(s). It multiples rapidly in the blood, the sporozoites migrate to the liver, invade live cell and asexually reproduce thousands of merozoites per cell. Afterward the merozoites exit the liver cell into the blood stream and invade the red blood cells. In the human red blood cell the merozoites develop into gametocytes (sexual forms of the parasite); the infected human red blood cell burst and releasing the developed gametocytes. Symptoms/Treatment When an individual is bitten by infected anopheles mosquito and eventually develop some or all of the following malaria symptoms. Intermittent high fever (febrile), a flu like fever, body aches with hot and cold stages, headache, nausea, shaking chills, sweating, weakness, hemolytic anemia in some case, coma or death. They’re several medications for the treatment of malaria, depending on individual tolerance and allergic reactions. Some of the medications include: chloroquine, malarone, mefloquine, quinine, doxycycline, clindamycin and other several “quine” drugs. Prophylactic use of medications, mosquito nets, proper sanitary condition and disposal of stagnant water serve as breeding ground are ways to prevent malaria Evolution of malaria resistance in sickle cell carriers Hemoglobin comprise of four protein subunits (tetramer), usual two beta and two alpha subunits. A mutation of the beta hemoglobin gene gives rise to sickle hemoglobin. Sickle cell disease (SCD) is an autosomal recessively inherited disorder of hemoglobin called sickle hemoglobin or hemoglobin S (HbS). It is caused by a single nucleotide substitution in the β globin gene on chromosome 11. The change in nucleotide sequence from G'T'''G to G'A'G resulting in substitution of '''Valine '(hydrophobic) for Glutamate (hydrophilic) amino acid. Contrary to normal life span of 120 days of red blood cells, abnormality of the beta globin distort the shape of the red blood cell into a sickle crescent or shape, thus the red blood cell die prematurely with 10-20 days leading to anemia in individual with homozygous recessive HbSS heterozygous HbS genes. If two carriers have a child,the child has a 25% percent probability of receiving two copies of the sickle form and having the anemia. Sickle cell anemia is deadly, yet the heterozygous allele is advantageous in malaria-infested region. As such approximately ten percent of African Americans are carriers, it predominantly afflict one racial group due to malaria. Heterozygote sickle cell carriers (HbS) are more resistant to malaria than individuals with normal hemoglobin or homozygous recessive (HbSS) hemoglobin. Because short life span (10 to 20 days) of the heterozygotes sickle cell carrier red blood cell, makes it difficult for the life cycle of the malaria parasite (10 to 18 days). The red blood cells or carrier rupture before the parasite complete it life cycle and in some cases if the life cycle of the malaria parasite is complete and able to cause malaria. The duration of the malaria symptoms last for few days, because the premature death of some of the red blood, leading to an end to the reproduction of the parasite and inability to affect new red blood cells. Thus, the carriers possess a stronger selective advantage against malaria over non carriers and are able to reproduce due to natural selection, leading to evolution of carrier alleles in the population References A case study of the effects of mutation: Sickle cell anemia. (n.d.). Retrieved November 19, 2014, from http://evolution.berkeley.edu/evolibrary/article/mutations_06 American Public Health Association (2008). Malaria. In DL Heymann, ed., Control of Communicable Diseases Manual, 19th ed., pp. 373–393. Washington, DC: American Public Health Association. Brunette, G.W., ed. CDC Health Information for International Travel 2012: The Yellow Book. New York: Oxford University Press, 2012. Gardner, M.,Hall N,Fung E,White O,Berriman M,Hyman RW,Carlton JM,Pain A,Nelson KE,Bowman S, et.al.(2002, October 3). Genome sequence of the human malaria parasite Plasmodium falciparum. Retrieved November 19, 2014, from http://www.ncbi.nlm.nih.gov/pubmed/12368864 Malaria-Cause. (n.d.). Cause of malaria.Retrieved November 19, 2014, from http://www.webmd.com/a-to-z-guides/malaria-cause Rediscovering Biology - Online Textbook: Unit 9 Human Evolution. (n.d.). Retrieved November 19, 2014, from http://www.learner.org/courses/biology/textbook/humev/humev_8.html What Is Sickle Cell Anemia? (2011, January 1). Retrieved November 19, 2014, from http://www.nhlbi.nih.gov/health/health-topics/topics/sca/